Note: This article was originally published with an incorrect version of the Acknowledgments, which appeared on p. 218 of the print version. The correct version of the Acknowledgments appeared on pp. 1–2. The corrected article is available below.

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Human Health Risk Assessment for Aluminium, Aluminium Oxide, and Aluminium Hydroxide

Literature regarding the biochemistry of aluminum and eight similar ions is reviewed. Close and hitherto unknown similarities were found. A hypothetical model is presented for the metabolism, based on documented direct observations of Al3+ and analogies from other ions. Main characteristics are low intestinal absorption, rapid urinary excretion, and slow tissue uptake, mostly in skeleton and reticuloendothelial cells. Intracellular Al3+ is probably first confined in the lysosomes but then slowly accumulates in the cell nucleus and chromatin. Large, long-lived cells, e.g., neurons, may be the most liable to this accumulation. In heterochromatin, Al3+ levels can be found comparable to those used in leather tannage. It is proposed that an accumulation may take place at a subcellular level without any significant increase in the corresponding tissue concentration. The possible effects of this accumulation are discussed. As Al3+ is neurotoxic, the brain metabolism is most interesting. The normal and the lethally toxic brain levels of Al3+ are well documented and differ only by a factor of 3-10. The normal brain uptake of Al3+ is estimated from data on intestinal uptake of Al3+ and brain uptake of radionuclides of similar ions administered intravenously. The uptake is very slow, 1 mg in 36 years, and is consistent with an assumption that Al3+ taken up by the brain cannot be eliminated and is therefore accumulated. The possibility that Al3+ may cause or contribute to some specific diseases, most of them related to aging, is discussed with the proposed metabolic picture in mind.

Metabolism and possible health effects of aluminum.

WITHIN THE LAST 30 years the mortality from burns and scalds has fallen. However, this change is largely relatable to the reduction of the death rate from burns and scalds covering 60% or less of the body's surface, and the more especially from those covering less than 50% (Table 1). Although burns covering more than 65% of the body are still regularly but not always fatal, the fact that, on a graph, the relationship of mortality to the size of burn is ogival is reason to believe that ultimately even burns covering 90% to 100% of the body will not always be lethal. Traumatic shock is no longer a significant contributing factor to the mortality rate. Even the shock attending thermal injuries covering 50% to 85% of the body is successfully treated by the provision of a sufficient quantity of a balanced solution of sodium salts, such as Hartmann's solution.*

Treatment of large human burns with 0.5 per cent silver nitrate solution.

: There are insufficient data to support a treatment standard treatment at this time. Guidelines - Adults and children with burns greater than 20% TBSA should undergo formal fluid resuscitation using estimates based on body size and surface area burned. - Common formulas used to initiate of resuscitation estimate a crystalloid need for 2 to 4 ml/kg body weight/%TBSA during the first 24 hours. - Fluid resuscitation,regardless of solution type or estimated need, should be titrated to maintain a urine output of approximately 0.5 1.0 ml/ kg/hr in adults and 1.0 1.5 ml/kg/hr in children. - Maintenance fluids should be administered to children in addition to their calculated fluid requirements caused by injury. - Increased volume requirements can be anticipated in patients with full-thickness injuries, inhalation injury, and a delay in resuscitation. Options - The addition of colloid-containing fluid following burn injury, especially after the first 12 to 24 hours postburn, may decrease overall fluid requirements.

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American Burn Association practice guidelines burn shock resuscitation.

Hypertrophic scar formation is a major clinical problem in the developing and industrialized injuries, and surgical procedures can give rise to exuberant scarring that resaults in permanent functional loss and the stigma of disfigurement. Figure 1 illustrates the scope of the problem. Annually, over 1 million people require treatment for burns in the United States [1], 2 million are injured in motor vehicle accidents [2], and over 34 million related surgical procedures are performed [3]. Although the incidence of hypertrophic scarring following these types of injuries is not known, it is a common outcome that creates a problem of enormous magnitude. Treatment of these cases is estimated to cost at least $4 billion per annum in the US alone [4]. The incidence of burns and traumatic injuries is even greater in the developing world [5]. This review will examine the process of hypertrophic scar formation, the results of current treatments, and areas likely to lead to significant advances in the field.



Figure 1

Complications of Hypertrophic Scarring

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Hypertrophic scar formation following burns and trauma: new approaches to treatment.

The adequate management of a serious burn demands the skill and knowledge of both the physician and the surgeon. By reason of the emergent character of most burn cases and because of lack of knowledge relative to the newer conceptions of the nature of the processes underlying a burn, treatment is usually regarded as exceedingly difficult and unsatisfactory. With the advance of industry, burns are becoming of greater frequency and consequently of greater importance to the practitioner. Their increased occurrence lays an obligation on the medical profession to become conversant with the fundamental conditions induced by a burn and to become familiar with the most efficient methods of treatment. It is not sufficient to treat the wounded area only. Much more important is the recognition of systemic effects and the immediate institution of proper treatment to combat these effects. "What does it profit a man if he dresses the wound

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The significance of anhydremia in extensive superficial burns

In extensive superficial burns involving considerable areas of the body's surface a rapid concentration of the blood occurs, and in our opinion this hitherto unconsidered factor is of the greatest importance in the development of the syndrome characteristic of burns. Concentrated blood is a factor which cannot well be left out of consideration in the study of any diseased condition in which it manifests itself. Marked concentration of the blood means a failing circulation, an inefficient oxygen carrier, oxygen starvation of the tissues, fall of temperature, and finally, suspension of vital activities. This viewpoint was initiated during the World War by the results of an extensive investigation of the action of the lethal war gases 1 which produce a noteworthy concentration of the blood as a result of the acute massive edema. Similar conditions obtain in certain cases of influenza. 2 On first consideration it may be difficult to correlate reactions in

Blood concentration changes in extensive superficial burns, and their significance for systemic treatment

Studies in carbohydrate metabolism i. the influence of hydrazine upon the organism, with special reference to the blood sugar content

Studies on the mechanism of water exchange in the animal organism

Studies in carbohydrate metabolism vi. the influence of thyreoparathyroidectomy upon the sugar content of the blood and the glycogen content of the liver

Frank P. Underhill

Papers

The significance of anhydremia in extensive superficial burns

Blood concentration changes in extensive superficial burns, and their significance for systemic treatment

Studies in carbohydrate metabolism i. the influence of hydrazine upon the organism, with special reference to the blood sugar content

Studies on the mechanism of water exchange in the animal organism

Studies in carbohydrate metabolism vi. the influence of thyreoparathyroidectomy upon the sugar content of the blood and the glycogen content of the liver